An Alzheimer Risk Gene May Not Be Responsible for Brain Plaques

When cognitively normal older subjects possess a newly identified gene variant associated with risk for late-onset Alzheimer's disease, they have less amyloid—the hallmark of Alzheimer's—in their brains than do cognitively normal older subjects without the variant. So reported Madhav Thambisetty, M.D., Ph.D., of the National Institute on Aging, and his colleagues online September 27 in Biological Psychiatry. 

What this means isn't clear, Thambisetty stated in an accompanying press release. But it could be that the gene variant—a variant of the complement receptor-1 gene—increases Alzheimer risk by a route other than increasing amyloid deposition in the brain. And while amyloid plaques seem to be the hallmark of Alzheimer's, a protein made by neurons, histone deacetylase 2, also seems to be involved in the Alzheimer's disease process. 

To read more about this finding, see Psychiatric News. Information about Alzheimer's disease in general can be found in a new American Psychiatric Publishing book, Clinical Manual of Alzheimer Disease and Other Dementias.

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